Intrinsic and extrinsic mechanisms contribute to maintain the JAK/STAT pathway aberrantly activated in T-type large granular lymphocyte leukemia.

@article{Teramo2013IntrinsicAE,
  title={Intrinsic and extrinsic mechanisms contribute to maintain the JAK/STAT pathway aberrantly activated in T-type large granular lymphocyte leukemia.},
  author={Antonella Teramo and Cristina Gattazzo and Francesca Passeri and Albana Lico and Giulia Tasca and Anna Cabrelle and V. Martini and Federica Frezzato and Valentina Trimarco and E. Lancaster Ave and Elisa Boscaro and Francesco Piazza and Monica Facco and Livio Trentin and Gianpietro Semenzato and Renato Zambello},
  journal={Blood},
  year={2013},
  volume={121 19},
  pages={3843-54, S1}
}
The JAK/STAT pathway is altered in T-cell large granular lymphocytic leukemia. In all patients, leukemic LGLs display upregulation of phosphorylated STAT3 (P-STAT3) that activates expression of many antiapoptotic genes. To investigate the mechanisms maintaining STAT3 aberrantly phosphorylated using transcriptional protein and functional assays, we analyzed interleukin (IL)-6 and suppressor of cytokine signaling-3 (SOCS3), 2 key factors of the JAK/STAT pathway that induce and inhibit STAT3… CONTINUE READING

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